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Article ; Online: Granulocytes subsets and their divergent functions in host resistance to Mycobacterium tuberculosis - a 'tipping-point' model of disease exacerbation.

Mayer-Barber, Katrin D

2023 Volume 84, Page(s) 102365

Abstract: Granulocytes are innate immune effector cells with essential functions in host resistance to bacterial infections. I will discuss emerging evidence that during Mycobacterium tuberculosis infection, counter-intuitively, eosinophils are host-protective ... ...

Abstract	Granulocytes are innate immune effector cells with essential functions in host resistance to bacterial infections. I will discuss emerging evidence that during Mycobacterium tuberculosis infection, counter-intuitively, eosinophils are host-protective while neutrophils are host detrimental. Additionally, I will propose a 'tipping-point' model in which neutrophils are an integral part of a feedforward loop driving tuberculosis disease exacerbation.
MeSH term(s)	Humans ; Mycobacterium tuberculosis ; Tuberculosis ; Neutrophils ; Eosinophils ; Immunity, Innate
Language	English
Publishing date	2023-07-10
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2023.102365
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Article ; Online: Signature required: The transcriptional response to tuberculosis.

Barry, Clifton E / Mayer-Barber, Katrin D

The Journal of experimental medicine

2021 Volume 218, Issue 12

Abstract: The majority of humans infected with Mycobacterium tuberculosis never experience clinical symptoms or signs, but predicting those who will remains out of reach. Here, we discuss recent studies that reveal patterns and pathways that determine who is at ... ...

Abstract	The majority of humans infected with Mycobacterium tuberculosis never experience clinical symptoms or signs, but predicting those who will remains out of reach. Here, we discuss recent studies that reveal patterns and pathways that determine who is at highest risk for progression.
MeSH term(s)	Gene Expression ; Genetic Predisposition to Disease ; Host-Pathogen Interactions/physiology ; Humans ; Latent Tuberculosis/genetics ; Mycobacterium tuberculosis/pathogenicity ; Tuberculosis/genetics ; Tuberculosis/microbiology ; Tuberculosis/transmission
Language	English
Publishing date	2021-11-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20211665
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Article ; Online: IRGM1 supports host defense against intracellular bacteria through suppression of type I interferon in mice.

Rai, Prashant / Sharpe, Martin / Ganta, Charan K / Baker, Paul J / Mayer-Barber, Katrin D / Fee, Brian E / Taylor, Gregory A / Fessler, Michael B

The Journal of clinical investigation

2023 Volume 133, Issue 21

MeSH term(s)	Animals ; Mice ; Bacteria ; Immunity, Innate ; Interferon Type I ; Macrophages/microbiology
Chemical Substances	Interferon Type I ; Ifi1 protein, mouse
Language	English
Publishing date	2023-11-01
Publishing country	United States
Document type	Letter
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI171982
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Article ; Online: Routemaps for Highly Effective Tuberculosis Vaccination.

Assmann, Maike / Mayer-Barber, Katrin D

Immunity

2019 Volume 52, Issue 2, Page(s) 219–221

Abstract: There is no highly effective tuberculosis vaccine. Darrah et al. (2020) and Tait et al. (2019) are setting new benchmarks for protection against infection and pulmonary disease by changing the route of vaccine delivery and by using a protein subunit ... ...

Abstract	There is no highly effective tuberculosis vaccine. Darrah et al. (2020) and Tait et al. (2019) are setting new benchmarks for protection against infection and pulmonary disease by changing the route of vaccine delivery and by using a protein subunit vaccine with a potent adjuvant.
MeSH term(s)	Humans ; Mycobacterium tuberculosis/immunology ; Tuberculosis ; Tuberculosis Vaccines ; Vaccination ; Vaccines, Subunit
Chemical Substances	Tuberculosis Vaccines ; Vaccines, Subunit
Language	English
Publishing date	2019-12-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2020.01.017
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Article ; Online: Mycobacterium tuberculosis inhibits the NLRP3 inflammasome activation via its phosphokinase PknF.

Rastogi, Shivangi / Ellinwood, Sarah / Augenstreich, Jacques / Mayer-Barber, Katrin D / Briken, Volker

PLoS pathogens

2021 Volume 17, Issue 7, Page(s) e1009712

Abstract: Mycobacterium tuberculosis (Mtb) has evolved to evade host innate immunity by interfering with macrophage functions. Interleukin-1β (IL-1β) is secreted by macrophages after the activation of the inflammasome complex and is crucial for host defense ... ...

Abstract	Mycobacterium tuberculosis (Mtb) has evolved to evade host innate immunity by interfering with macrophage functions. Interleukin-1β (IL-1β) is secreted by macrophages after the activation of the inflammasome complex and is crucial for host defense against Mtb infections. We have previously shown that Mtb is able to inhibit activation of the AIM2 inflammasome and subsequent pyroptosis. Here we show that Mtb is also able to inhibit host cell NLRP3 inflammasome activation and pyroptosis. We identified the serine/threonine kinase PknF as one protein of Mtb involved in the NLRP3 inflammasome inhibition, since the pknF deletion mutant of Mtb induces increased production of IL-1β in bone marrow-derived macrophages (BMDMs). The increased production of IL-1β was dependent on NLRP3, the adaptor protein ASC and the protease caspase-1, as revealed by studies performed in gene-deficient BMDMs. Additionally, infection of BMDMs with the pknF deletion mutant resulted in increased pyroptosis, while the IL-6 production remained unchanged compared to Mtb-infected cells, suggesting that the mutant did not affect the priming step of inflammasome activation. In contrast, the activation step was affected since potassium efflux, chloride efflux and the generation of reactive oxygen species played a significant role in inflammasome activation and subsequent pyroptosis mediated by the Mtb pknF mutant strain. In conclusion, we reveal here that the serine/threonine kinase PknF of Mtb plays an important role in innate immune evasion through inhibition of the NLRP3 inflammasome.
MeSH term(s)	Animals ; Host-Pathogen Interactions/immunology ; Immune Evasion/immunology ; Inflammasomes/immunology ; Mice ; Mycobacterium tuberculosis/immunology ; Mycobacterium tuberculosis/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology ; Protein Serine-Threonine Kinases/immunology ; Protein Serine-Threonine Kinases/metabolism ; Tuberculosis/immunology ; Tuberculosis/metabolism
Chemical Substances	Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; PknF protein, Mycobacterium tuberculosis (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-07-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1009712
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Article ; Online: A TNF-IL-1 circuit controls Yersinia within intestinal pyogranulomas.

Matsuda, Rina / Sorobetea, Daniel / Zhang, Jenna / Peterson, Stefan T / Grayczyk, James P / Yost, Winslow / Apenes, Nicolai / Kovalik, Maria E / Herrmann, Beatrice / O'Neill, Rosemary J / Bohrer, Andrea C / Lanza, Matthew / Assenmacher, Charles-Antoine / Mayer-Barber, Katrin D / Shin, Sunny / Brodsky, Igor E

The Journal of experimental medicine

2024 Volume 221, Issue 3

Abstract: Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. We previously reported that Yersinia pseudotuberculosis colonizes the ... ...

Abstract	Tumor necrosis factor (TNF) is a pleiotropic inflammatory cytokine that mediates antimicrobial defense and granuloma formation in response to infection by numerous pathogens. We previously reported that Yersinia pseudotuberculosis colonizes the intestinal mucosa and induces the recruitment of neutrophils and inflammatory monocytes into organized immune structures termed pyogranulomas (PG) that control Yersinia infection. Inflammatory monocytes are essential for the control and clearance of Yersinia within intestinal PG, but how monocytes mediate Yersinia restriction is poorly understood. Here, we demonstrate that TNF signaling in monocytes is required for bacterial containment following enteric Yersinia infection. We further show that monocyte-intrinsic TNFR1 signaling drives the production of monocyte-derived interleukin-1 (IL-1), which signals through IL-1 receptors on non-hematopoietic cells to enable PG-mediated control of intestinal Yersinia infection. Altogether, our work reveals a monocyte-intrinsic TNF-IL-1 collaborative inflammatory circuit that restricts intestinal Yersinia infection.
MeSH term(s)	Humans ; Interleukin-1 ; Yersinia ; Yersinia Infections ; Yersinia pseudotuberculosis ; Tumor Necrosis Factor-alpha ; Monocytes
Chemical Substances	Interleukin-1 ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20230679
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Article ; Online: Co-infection of mice with SARS-CoV-2 and

Baker, Paul J / Amaral, Eduardo P / Castro, Ehydel / Bohrer, Andrea C / Torres-Juárez, Flor / Jordan, Cassandra M / Nelson, Christine E / Barber, Daniel L / Johnson, Reed F / Hilligan, Kerry L / Mayer-Barber, Katrin D

Frontiers in immunology

2023 Volume 14, Page(s) 1240419

Abstract: Viral co-infections have been implicated in worsening tuberculosis (TB) and during the COVID-19 pandemic, the global rate of TB-related deaths has increased for the first time in over a decade. We and others have previously shown that a resolved prior or ...

Abstract	Viral co-infections have been implicated in worsening tuberculosis (TB) and during the COVID-19 pandemic, the global rate of TB-related deaths has increased for the first time in over a decade. We and others have previously shown that a resolved prior or concurrent influenza A virus infection in
MeSH term(s)	Mice ; Animals ; Humans ; Mycobacterium tuberculosis ; SARS-CoV-2 ; Coinfection ; Pandemics ; COVID-19 ; Mice, Transgenic ; Interferon Type I ; Mice, Inbred C57BL
Chemical Substances	K-18 conjugate ; Interferon Type I
Language	English
Publishing date	2023-09-01
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1240419
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Article: Blood and Site of Disease Inflammatory Profiles Differ in Patients With Pericardial Tuberculosis and Human Immunodeficiency Virus Type 1.

Mutavhatsindi, Hygon / Du Bruyn, Elsa / Ruzive, Sheena / Howlett, Patrick / Cerrone, Maddalena / Sher, Alan / Mayer-Barber, Katrin D / Barber, Daniel L / Ntsekhe, Mpiko / Wilkinson, Robert J / Riou, Catherine

Open forum infectious diseases

2023 Volume 10, Issue 3, Page(s) ofad128

Abstract: Background: To better understand the pathogenesis of pericardial tuberculosis (PCTB), we sought to characterize the systemic inflammatory profile in people with human immunodeficiency virus type 1 (HIV-1) with latent TB infection (LTBI), pulmonary TB ( ... ...

Abstract	Background: To better understand the pathogenesis of pericardial tuberculosis (PCTB), we sought to characterize the systemic inflammatory profile in people with human immunodeficiency virus type 1 (HIV-1) with latent TB infection (LTBI), pulmonary TB (PTB), or PCTB. Methods: Using Luminex, we measured the concentration of 39 analytes in pericardial fluid (PCF) and paired plasma from 18 PCTB participants, and plasma from 16 LTBI and 20 PTB participants. Follow-up plasma samples were also obtained from PTB and PCTB participants. HLA-DR expression on Results: Assessment of the overall systemic inflammatory profile by principal component analysis showed that the inflammatory profile of active TB participants was distinct from the LTBI group, while PTB patients could not be distinguished from those with PCTB. When comparing the inflammatory profile between PCF and paired blood, we found that the concentrations of most analytes (25/39) were elevated at site of disease. However, the inflammatory profile in PCF partially mirrored inflammatory events in the blood. After TB treatment completion, the overall plasma inflammatory profile reverted to that observed in the LTBI group. Lastly, HLA-DR expression showed the best performance for TB diagnosis compared to previously described biosignatures built from soluble markers. Conclusions: Our results show that the inflammatory profile in blood was comparable between PTB and PCTB. However, at the site of infection (PCF), inflammation was significantly elevated compared to blood. Additionally, our data emphasize the potential role of HLA-DR expression as a biomarker for TB diagnosis.
Language	English
Publishing date	2023-03-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2757767-3
ISSN	2328-8957
ISSN	2328-8957
DOI	10.1093/ofid/ofad128
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Article ; Online: Clash of the Cytokine Titans: counter-regulation of interleukin-1 and type I interferon-mediated inflammatory responses.

Mayer-Barber, Katrin D / Yan, Bo

Cellular & molecular immunology

2016 Volume 14, Issue 1, Page(s) 22–35

Abstract: Over the past decades the notion of 'inflammation' has been extended beyond the original hallmarks of rubor (redness), calor (heat), tumor (swelling) and dolor (pain) described by Celsus. We have gained a more detailed understanding of the cellular ... ...

Abstract	Over the past decades the notion of 'inflammation' has been extended beyond the original hallmarks of rubor (redness), calor (heat), tumor (swelling) and dolor (pain) described by Celsus. We have gained a more detailed understanding of the cellular players and molecular mediators of inflammation which is now being applied and extended to areas of biomedical research such as cancer, obesity, heart disease, metabolism, auto-inflammatory disorders, autoimmunity and infectious diseases. Innate cytokines are often central components of inflammatory responses. Here, we discuss how the type I interferon and interleukin-1 cytokine pathways represent distinct and specialized categories of inflammatory responses and how these key mediators of inflammation counter-regulate each other.
MeSH term(s)	Animals ; Cytokines/metabolism ; Humans ; Inflammation/metabolism ; Inflammation/pathology ; Interferon Type I/metabolism ; Interleukin-1/metabolism ; Models, Biological
Chemical Substances	Cytokines ; Interferon Type I ; Interleukin-1
Language	English
Publishing date	2016-06-06
Publishing country	China
Document type	Journal Article ; Review ; Research Support, N.I.H., Intramural
ZDB-ID	2435097-7
ISSN	2042-0226 ; 1672-7681
ISSN (online)	2042-0226
ISSN	1672-7681
DOI	10.1038/cmi.2016.25
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Article: The inflammatory microenvironment of the lung at the time of infection governs innate control of SARS-CoV-2 replication.

Baker, Paul J / Bohrer, Andrea C / Castro, Ehydel / Amaral, Eduardo P / Snow-Smith, Maryonne / Torres-Juárez, Flor / Gould, Sydnee T / Queiroz, Artur T L / Fukutani, Eduardo R / Jordan, Cassandra M / Khillan, Jaspal S / Cho, Kyoungin / Barber, Daniel L / Andrade, Bruno B / Johnson, Reed F / Hilligan, Kerry L / Mayer-Barber, Katrin D

bioRxiv : the preprint server for biology

2024

Abstract: SARS-CoV-2 infection leads to vastly divergent clinical outcomes ranging from asymptomatic infection to fatal disease. Co-morbidities, sex, age, host genetics and vaccine status are known to affect disease severity. Yet, how the inflammatory milieu of ... ...

Abstract	SARS-CoV-2 infection leads to vastly divergent clinical outcomes ranging from asymptomatic infection to fatal disease. Co-morbidities, sex, age, host genetics and vaccine status are known to affect disease severity. Yet, how the inflammatory milieu of the lung at the time of SARS-CoV-2 exposure impacts the control of viral replication remains poorly understood. We demonstrate here that immune events in the mouse lung closely preceding SARS-CoV-2 infection significantly impact viral control and we identify key innate immune pathways required to limit viral replication. A diverse set of pulmonary inflammatory stimuli, including resolved antecedent respiratory infections with
Language	English
Publishing date	2024-03-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.27.586885
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